Lupus nephritis (LN) is a representative manifestation in systemic lupus erythematosus (SLE). Some studies have shown that myeloid-derived suppressor cells (MDSCs) play a vital role in the regulation of the SLE process. MDSC infiltration in the kidney as well as inflammation and oxidative stress provokes the acceleration and deterioration of LN. Nuclear factor E2-related factor 2 (Nrf2) is thought to be a major regulator of the antioxidant response. Baicalein is a flavonoid with known anti-inflammatory effects and antioxidant response. However, the effects of baicalein on MDSCs, inflammation, and oxidative stress are not evaluated in the development of pristane-induced LN in mice. The renoprotective effect of baicalein was detected in a pristane-induced lupus mice model. NLRP3 inflammasome activation and NF-κB phosphorylation as well as reactive oxygen species (ROS) production and Nrf2 activation were examined. The percentages and function changes of MDSCs were measured. The possible mechanisms of the underlying effects of baicalein on ROS production and signaling pathways of Nrf2/heme-oxygenase (HO)-1, NLRP3 inflammasome, and NF-κB phosphorylation in lipopolysaccharide (LPS)-primed MDSCs were analyzed. Baicalein reduced proteinuria and attenuated renal function impairment and renal histopathology including intrinsic cell proliferation, cellular crescents, and podocyte injury as well as glomerulonephritis activity in lupus mice. Moreover, baicalein downregulated the activation of NLRP3 inflammasome and levels of ROS or NF-κB phosphorylation, and it enhanced Nrf2 activation. Of note, baicalein inhibited the expansion of MDSCs and improved the function of MDSCs in lupus mice. Through analyzing LPS-primed MDSCs in vitro, baicalein was found to exhibit cytoprotective effects coincident with the induction of Nrf2/HO-1 signaling and the suppression of the NLRP3 inflammasome. The data show that baicalein alleviates the symptoms of pristane-induced LN and suggest that the alleviation may be attributed to inhibition of MDSC expansion and regulation of the balance of the Nrf2/HO-1 signal and NLRP3 expression in MDSCs.

/pdf/baicalein-ameliorates-pristane-induced-lupus-nephritis-via-4v4n4dubws.pdf

Baicalein ameliorates pristane-induced lupus nephritis via activating Nrf2/HO-1 in myeloid-derived suppressor cells

Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy, is characterized by a reduction in NO bioavailability. Oxidative stress, which is the main pathogenic factor in diabetes, is one of the major triggers of endothelial dysfunction through the reduction in NO. In this review, we summarize the four sources of ROS in the diabetic vasculature and the underlying molecular mechanisms by which the pathogenic factors hyperglycaemia, hyperlipidaemia, adipokines and insulin resistance induce oxidative stress in endothelial cells in the context of diabetes. In addition, we discuss oxidative stress-targeted interventions, including hypoglycaemic drugs, antioxidants and lifestyle interventions, and their effects on diabetes-induced endothelial dysfunction. In summary, our review provides comprehensive insight into the roles of oxidative stress in diabetes-induced endothelial dysfunction. 

pdf/the-role-of-oxidative-stress-in-diabetes-mellitus-induced-1h7v4lwqhz.pdf

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

Baicalein: A metabolite with promising antineoplastic activity

POEMS syndrome is a rare para-neoplastic syndrome secondary to a plasma cell dyscrasia. Effective treatment can control the disease-related symptom complex. We describe the clinical outcome of autologous stem cell transplantation for patients with POEMS syndrome, determining the impact of patient- and disease-specific factors on prognosis. One hundred and twenty-seven patients underwent an autologous stem cell transplantation between 1997-2010 with a median age of 50 years (range 26-69 years). Median time from diagnosis to autologous stem cell transplantation was 7.5 months with 32% of patients receiving an autologous stem cell transplantation more than 12 months from diagnosis. Engraftment was seen in 97% patients and engraftment syndrome was documented in 23% of autologous stem cell transplantation recipients. Hematologic response was characterized as complete response in 48.5%, partial response in 20.8%, less than partial repsonse in 30.7%. With a median follow up of 48 months (95%CI: 38.3, 58.6), 90% of patients are alive and 16.5% of patients have progressed. The 1-year non-relapse mortality was 3.3%. The 3-year probabilities of progression-free survival and overall survival are 84% and 94%, respectively, with 5-year probabilities of progression-free survival and overall survival of 74% and 89%. In a cohort of graft recipients, detailed organ-specific symptom response demonstrated clear symptom benefit after autologous stem cell transplantation especially in relation to neurological symptom control. The data analyzed in this study demonstrate the clinical utility of autologous stem cell transplantation for patients with POEMS syndrome.

High-dose therapy and autologous stem cell transplantation in patients with POEMS syndrome: a retrospective study of the Plasma Cell Disorder sub-committee of the Chronic Malignancy Working Party of the European Society for Blood & Marrow Transplantation

Abstract Research into the potential benefits of artificial intelligence for comprehending the intricate biology of cancer has grown as a result of the widespread use of deep learning and machine learning in the healthcare sector and the availability of highly specialized cancer datasets. Here, we review new artificial intelligence approaches and how they are being used in oncology. We describe how artificial intelligence might be used in the detection, prognosis, and administration of cancer treatments and introduce the use of the latest large language models such as ChatGPT in oncology clinics. We highlight artificial intelligence applications for omics data types, and we offer perspectives on how the various data types might be combined to create decision-support tools. We also evaluate the present constraints and challenges to applying artificial intelligence in precision oncology. Finally, we discuss how current challenges may be surmounted to make artificial intelligence useful in clinical settings in the future. 

Novel research and future prospects of artificial intelligence in cancer diagnosis and treatment

Although the response rates of chemotherapy in patients with acute T-lymphoblastic leukemia (T-ALL) have improved significantly, the outcome of these patients is still poor. Previous studies suggested that baicalein could inhibit the growth of several cancers, while its effect on T-ALL cells remains unclear. We used Jurkat cells as an in vitro model of T-ALL. Cell counting kit-8 assay and cytometric analysis with Annexin V-FITC/PI double staining were used to investigate the proliferation and apoptosis of Jurkat cells treated with increasing concentration of baicalein for indicated time. RT-PCR and western blotting was used to test the expression of Wnt/β-catenin associated genes and proteins. In cell viability assay, baicalein could inhibit the proliferation of Jurkat cells both in dose- and time-dependent manners. In cell apoptosis assay, baicalein could stimulate apoptosis of Jurkat cells both in dose- and time-dependent manners. Moreover, we demonstrated that baicalein could down-regulated the mRNA and protein levels of β-catenin and its widely accepted downstream targets (c-Myc, cyclin D1, and Axin2) in dose-dependent manners. These results proved that baicalein might be a potential choice for the treatment of T-ALL.

Baicalein suppresses the proliferation of acute T-lymphoblastic leukemia Jurkat cells by inhibiting the Wnt/β-catenin signaling.

Baicalein suppresses the proliferation of acute T-lymphoblastic

BACKGROUND Baicalein can suppress the growth of multiple tumors, including multiple myeloma (MM), but the exact mechanisms remains elusive. Here, we investigated the exact mechanisms of the anti-myeloma activity of baicalein. MATERIAL AND METHODS Proliferation and rates of apoptosis of myeloma U266 cells exposed to baicalein were detected. Microarray, polymerase chain reaction (PCR) assay, and Western blot analysis were applied to evaluate the mRNA and protein levels of associated molecules. Survival analysis of IKZF1 and IKZF3 was conducted as well. RESULTS Baicalein suppressed the growth and stimulated apoptosis of myeloma U266 cells in a dose- and time-dependent way. Baicalein increased mRNA level of CRBN, and further studies suggested that baicalein downregulated IKZF1 and IKZF3 on a post-transcriptional level. Although the differences did not reach statistical significance, IKZF1 and IKZF3 were associated with poor overall survival. CONCLUSIONS Our results suggest that baicalein suppresses the growth and promotes apoptosis of myeloma U266 cells through downregulating IKZF1 and IKZF3. Baicalein increased the expression of CRBN, which might exert a reversion effect on resistance of IMiDs. MM patients in IKZF1 and IKZF3 low-expression groups had better overall survival than those in IKZF1 and IKZF3 high-expression groups. Thus, the present results indicate that baicalein might be a therapeutic choice for targeting IKZF1 and IKZF3.

/pdf/baicalein-inhibits-proliferation-of-myeloma-u266-cells-by-21r7q553ql.pdf

Baicalein Inhibits Proliferation of Myeloma U266 Cells by Downregulating IKZF1 and IKZF3.

Dear Editor, A 32-year-old woman was admitted because of progressive numbness in the lower limbs for 15 months, accompanied with pains in the breastbone, spine, and pelvis for 6 months before hospitalization. There was no prior history of exposure to neurologic toxins and no family history of neuropathy. Physical examination revealed splenomegaly, and no hyperpigmentation or other skin changes were observed. Neurological examination demonstrated moderate sensory disturbance of both lower limbs, with disappearance of deep tendon reflexes. Laboratory analysis showed that full blood count and urine routine test are normal. Other normal or negative results include hepatic and renal functions test, folate and VitB12 levels, and auto-antibody screen. Ophthalmoscopy revealed bilateral papilledema. Endocrinologic investigations showed low levels of FT3, FT4, testosterone, and estrogen. Electromyographic analysis demonstrated peripheral motor and sensory nerves demyelinating lesions in upper and lower limbs. Multiple osteosclerotic lesions in ribs, breastbone, spine, and pelvis were disclosed by CT scan (Fig. 1), together with a few lytic lesions in pelvis. Monoclonal IgG (κ) (20.3 g/l)(normal, 7.0–17.0 g/l) was detected in the serum by electrophoresis. There was no Bence-Jones proteinuria. Bone marrow aspiration revealed 2% of mature plasma cell with normal cytogenetics. Normal levels of protein, glucose and cells were detected in the cerebrospinal fluid (CSF). The patient met the criteria for the diagnosis of POEMS syndrome described by Dispenzieri [1]. She was initially treated with two cycles of chemotherapy with MP regimen (melphalan 6 mg/day days 1–7, Dexamethasone 40 mg/day, days 1–4, days 9–12, days 17–20). A minor improvement of numbness in the lower limbs was observed after chemotherapy, with disappearance of splenomegaly and papilledema, but the patient started to present with mild distal weakness of both lower limbs and toes. Bone pains in the breastbone, spine, and pelvis remained, but were stable. As she developed motor deficiency despite systemic chemotherapy, 5 months after diagnosis, she received autologous peripheral blood stem cell transplantation (autoPBSCT). Peripheral blood stem cell collection was performed after mobilization by chemotherapy (intravenous cyclophosphamide 60 mg/kg/day × 2 days), plus subcutaneous granulocyte colony-stimulating factor (rhG-CSF, 5 mg/kg/day) 6 days after chemotherapy and lasted for 3 days. The number of collected mononuclear cells (MNC) was 6.70×10/kg, and the CD34 cells were 7.51×10/kg. High-dose chemotherapy and autoPBSCT were performed 44 days after PBSC collection. She was conditioned using 200 mg/m melphalan, and the PBSC were infused 3 days later. Standard supportive care with prophylactic antibiotics was used before transplantation. Growth factor support was provided 3 days after stem cell transfusion. The transplantation course was uneventful except for a transient neutropenic fever and mucositis, which were settled with broad-spectrum antibacterial therapy. The patient was engrafted and the time to neutrophil count above 0.5×10/ l and platelets above 20×10/l was +10 and +11 days, respectively. Numbness in lower limbs improved gradually, and the area of sensory disturbance of numbness was limited in the bottoms of feet 6 months after transplantation, although Ann Hematol (2008) 87:247–248 DOI 10.1007/s00277-007-0379-2

Autologous peripheral blood stem cell transplantation in a patient with POEMS syndrome.

Essential thrombocythemia (ET) is an uncommon situation in which the body produces too many platelets. This can cause blood clots anywhere in the body and results in various symptoms and even strokes or heart attacks. Removing excessive platelets using acoustofluidic methods receives extensive attention due to their high efficiency and high yield. While the damage to the remaining cells, such as erythrocytes and leukocytes is yet evaluated. Existing cell damage evaluation methods usually require cell staining, which are time-consuming and labor-intensive. In this paper, we investigate cell damage by optical time-stretch (OTS) imaging flow cytometry with high throughput and in a label-free manner. Specifically, we first image the erythrocytes and leukocytes sorted by acoustofluidic sorting chip with different acoustic wave powers and flowing speed using OTS imaging flow cytometry at a flowing speed up to 1 m/s. Then, we employ machine learning algorithms to extract biophysical phenotypic features from the cellular images, as well as to cluster and identify images. The results show that both the errors of the biophysical phenotypic features and the proportion of abnormal cells are within 10% in the undamaged cell groups, while the errors are much greater than 10% in the damaged cell groups, indicating that acoustofluidic sorting causes little damage to the cells within the appropriate acoustic power, agreeing well with clinical assays. Our method provides a novel approach for high-throughput and label-free cell damage evaluation in scientific research and clinical settings. This article is protected by copyright. All rights reserved.

Cell damage evaluation by intelligent imaging flow cytometry.

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